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Object Bcl-2 plays a key role in the downregulation of apoptosis and proliferation and leads to increased chemoresistance in glioblastoma multiforme (GBM). The authors investigated the role of a common regulatory single-nucleotide polymorphism (−938C>A), which is located in the inhibitory P2 promoter of BCL2. Methods Data from 160 patients suffering from GBM were retrospectively evaluated. Study inclusion criteria consisted of available DNA and, in patients still alive, a follow-up of at least 24 months. Results were analyzed with respect to the basic clinical data, type of surgical intervention (gross-total resection [GTR] versus stereotactic biopsy [SB]), adjuvant therapy, MGMT promoter methylation, and survival at the 2-year follow-up. Results At the 2-year follow-up, 127 (79.4%) of the 160 patients had died. Kaplan-Meier curves revealed a significantly higher rate of survival for homo- and heterozygous C-allele carriers (p = 0.031). In the GTR group, the survival rate was 47.1% for homozygous C-allele carriers, 32.0% for heterozygous C-allele carriers, and only 21.4% for homozygous A-allele carriers (p = 0.024). The SB group showed no genotype-dependent differences. Multivariable Cox regression revealed that the BCL2 (−938AA) genotype was an independent negative prognostic factor for 2-year survival in the GTR group according to the BCL2 (−938CC) genotype reference group (hazard ratio 2.50, 95% CI 1.14–5.48, p = 0.022). Conclusions These results suggested that the (−938C>A) polymorphism is a survival prognosticator as well as a marker for a high-risk group among patients with GBM who underwent GTR.

Object In this study, the authors' goal was to analyze a series of patients treated microsurgically for an anterior clinoid process (ACP) meningioma in regard to long-term functional outcome. Methods The authors retrospectively analyzed clinical data in a consecutive series of 106 patients who underwent microsurgical treatment for an ACP meningioma at 2 neurosurgical institutions between 1987 and 2005. The main presenting symptoms of the 84 female and 22 male patients (mean age 56 years) were visual impairment in 54% and headache in 28%. Physical examination revealed decreased visual acuity in 49% and a visual field deficit in 26%. Tumors were primarily resected via a pterional approach. Meningioma extensions invading the cavernous sinus, present in 29% of the patients, were not removed. Complete tumor resection (Simpson Grade I and II) was achieved in 59% of the cases. Results Postoperatively, visual acuity improved in 40%, was unchanged in 46%, and deteriorated in 14%. A new oculomotor palsy was observed in 8 patients (8%). Clinical and MR imaging data were available in 95 patients for a mean postsurgical period of 6.9 years (1.5–18 years) and revealed tumor recurrence in 10% and tumor progression after subtotal resection in 38%. Clinical deterioration on long-term follow-up consisting primarily of ophthalmological deficits was observed in 14% of the cases. Conclusions Acceptable functional results can be achieved after microsurgical resection of ACP meningiomas; however, long-term treatment remains challenging due to a high tumor recurrence and progression rate.

Bcl-2 plays a key role in the downregulation of apoptosis and proliferation and leads to increased chemoresistance in glioblastoma multiforme (GBM). The authors investigated the role of a common regulatory single-nucleotide polymorphism (-938CA), which is located in the inhibitory P2 promoter of BCL2.Data from 160 patients suffering from GBM were retrospectively evaluated. Study inclusion criteria consisted of available DNA and, in patients still alive, a follow-up of at least 24 months. Results were analyzed with respect to the basic clinical data, type of surgical intervention (gross-total resection [GTR] versus stereotactic biopsy [SB]), adjuvant therapy, MGMT promoter methylation, and survival at the 2-year follow-up.At the 2-year follow-up, 127 (79.4%) of the 160 patients had died. Kaplan-Meier curves revealed a significantly higher rate of survival for homo- and heterozygous C-allele carriers (p = 0.031). In the GTR group, the survival rate was 47.1% for homozygous C-allele carriers, 32.0% for heterozygous C-allele carriers, and only 21.4% for homozygous A-allele carriers (p = 0.024). The SB group showed no genotype-dependent differences. Multivariable Cox regression revealed that the BCL2 (-938AA) genotype was an independent negative prognostic factor for 2-year survival in the GTR group according to the BCL2 (-938CC) genotype reference group (hazard ratio 2.50, 95% CI 1.14-5.48, p = 0.022).These results suggested that the (-938CA) polymorphism is a survival prognosticator as well as a marker for a high-risk group among patients with GBM who underwent GTR.